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Alteration of hippocampal cell proliferation in mice lacking the beta 2 subunit of the neuronal nicotinic acetylcholine receptor.

Abstract Adult hippocampal neurogenesis declines with age in parallel with decreased performance on a variety of hippocampal-dependent tasks. We measured the rate of cellular proliferation in the hippocampus of mice lacking the beta 2-subunit of the nicotinic acetylcholine receptor (beta 2-/- mice) at three ages: young adult (3 months old), fully adult (7-10 months old), and aged (22-24 months old). Consistent with previous studies, we observed an age-related decline in hippocampal proliferation in both groups. However, in fully adult beta 2-/- mice a 43% reduction of granule cell proliferation was detected compared to age-matched controls. This was accompanied by a significant decrease in dentate gyrus area/section and the length of the granule cell layer in beta 2-/- mice. These alterations were not the result of a change in plasma corticosterone levels or expression of the neurotrophic factor BDNF in the dentate gyrus, two known regulators of hippocampal cell proliferation. Similarly, there was no increase in gliosis, abnormal myelination, or apoptotic cell death in the beta 2-/- animals, although there was a significant shift in the location of apoptotic cells in the dentate gyrus indicative of a change in neuronal survival. These results suggest that the beta 2-subunit containing nicotinic acetylcholine receptors play an important role in regulating cell proliferation in the hippocampus and that endogenous acetylcholine may act to oppose the negative effects of normal aging and stress on cellular proliferation.
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Authors

Mayor MeshTerms
Keywords
Journal Title synapse (new york, n.y.)
Publication Year Start
%A Harrist, Alexia; Beech, Robert D.; King, Sarah L.; Zanardi, Alessio; Cleary, Muriel A.; Caldarone, Barbara J.; Eisch, Amelia; Zoli, Michele; Picciotto, Marina R.
%T Alteration of hippocampal cell proliferation in mice lacking the beta 2 subunit of the neuronal nicotinic acetylcholine receptor.
%J Synapse (New York, N.Y.), vol. 54, no. 4, pp. 200-206
%D 12/2004
%V 54
%N 4
%M eng
%B Adult hippocampal neurogenesis declines with age in parallel with decreased performance on a variety of hippocampal-dependent tasks. We measured the rate of cellular proliferation in the hippocampus of mice lacking the beta 2-subunit of the nicotinic acetylcholine receptor (beta 2-/- mice) at three ages: young adult (3 months old), fully adult (7-10 months old), and aged (22-24 months old). Consistent with previous studies, we observed an age-related decline in hippocampal proliferation in both groups. However, in fully adult beta 2-/- mice a 43% reduction of granule cell proliferation was detected compared to age-matched controls. This was accompanied by a significant decrease in dentate gyrus area/section and the length of the granule cell layer in beta 2-/- mice. These alterations were not the result of a change in plasma corticosterone levels or expression of the neurotrophic factor BDNF in the dentate gyrus, two known regulators of hippocampal cell proliferation. Similarly, there was no increase in gliosis, abnormal myelination, or apoptotic cell death in the beta 2-/- animals, although there was a significant shift in the location of apoptotic cells in the dentate gyrus indicative of a change in neuronal survival. These results suggest that the beta 2-subunit containing nicotinic acetylcholine receptors play an important role in regulating cell proliferation in the hippocampus and that endogenous acetylcholine may act to oppose the negative effects of normal aging and stress on cellular proliferation.
%K Aging, Animals, Apoptosis, Cell Division, Female, Gliosis, Hippocampus, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Neurons, Receptors, Nicotinic
%P 200
%L 206
%Y 10.1002/syn.20081
%W PHY
%G AUTHOR
%R 2004.......54..200H

@Article{Harrist2004,
author="Harrist, Alexia
and Beech, Robert D.
and King, Sarah L.
and Zanardi, Alessio
and Cleary, Muriel A.
and Caldarone, Barbara J.
and Eisch, Amelia
and Zoli, Michele
and Picciotto, Marina R.",
title="Alteration of hippocampal cell proliferation in mice lacking the beta 2 subunit of the neuronal nicotinic acetylcholine receptor.",
journal="Synapse (New York, N.Y.)",
year="2004",
month="Dec",
day="15",
volume="54",
number="4",
pages="200--206",
keywords="Aging",
keywords="Animals",
keywords="Apoptosis",
keywords="Cell Division",
keywords="Female",
keywords="Gliosis",
keywords="Hippocampus",
keywords="Male",
keywords="Mice",
keywords="Mice, Inbred C57BL",
keywords="Mice, Knockout",
keywords="Neurons",
keywords="Receptors, Nicotinic",
abstract="Adult hippocampal neurogenesis declines with age in parallel with decreased performance on a variety of hippocampal-dependent tasks. We measured the rate of cellular proliferation in the hippocampus of mice lacking the beta 2-subunit of the nicotinic acetylcholine receptor (beta 2-/- mice) at three ages: young adult (3 months old), fully adult (7-10 months old), and aged (22-24 months old). Consistent with previous studies, we observed an age-related decline in hippocampal proliferation in both groups. However, in fully adult beta 2-/- mice a 43\% reduction of granule cell proliferation was detected compared to age-matched controls. This was accompanied by a significant decrease in dentate gyrus area/section and the length of the granule cell layer in beta 2-/- mice. These alterations were not the result of a change in plasma corticosterone levels or expression of the neurotrophic factor BDNF in the dentate gyrus, two known regulators of hippocampal cell proliferation. Similarly, there was no increase in gliosis, abnormal myelination, or apoptotic cell death in the beta 2-/- animals, although there was a significant shift in the location of apoptotic cells in the dentate gyrus indicative of a change in neuronal survival. These results suggest that the beta 2-subunit containing nicotinic acetylcholine receptors play an important role in regulating cell proliferation in the hippocampus and that endogenous acetylcholine may act to oppose the negative effects of normal aging and stress on cellular proliferation.",
issn="0887-4476",
doi="10.1002/syn.20081",
url="http://www.ncbi.nlm.nih.gov/pubmed/15472930",
language="eng"
}

%0 Journal Article
%T Alteration of hippocampal cell proliferation in mice lacking the beta 2 subunit of the neuronal nicotinic acetylcholine receptor.
%A Harrist, Alexia
%A Beech, Robert D.
%A King, Sarah L.
%A Zanardi, Alessio
%A Cleary, Muriel A.
%A Caldarone, Barbara J.
%A Eisch, Amelia
%A Zoli, Michele
%A Picciotto, Marina R.
%J Synapse (New York, N.Y.)
%D 2004
%8 Dec 15
%V 54
%N 4
%@ 0887-4476
%G eng
%F Harrist2004
%X Adult hippocampal neurogenesis declines with age in parallel with decreased performance on a variety of hippocampal-dependent tasks. We measured the rate of cellular proliferation in the hippocampus of mice lacking the beta 2-subunit of the nicotinic acetylcholine receptor (beta 2-/- mice) at three ages: young adult (3 months old), fully adult (7-10 months old), and aged (22-24 months old). Consistent with previous studies, we observed an age-related decline in hippocampal proliferation in both groups. However, in fully adult beta 2-/- mice a 43% reduction of granule cell proliferation was detected compared to age-matched controls. This was accompanied by a significant decrease in dentate gyrus area/section and the length of the granule cell layer in beta 2-/- mice. These alterations were not the result of a change in plasma corticosterone levels or expression of the neurotrophic factor BDNF in the dentate gyrus, two known regulators of hippocampal cell proliferation. Similarly, there was no increase in gliosis, abnormal myelination, or apoptotic cell death in the beta 2-/- animals, although there was a significant shift in the location of apoptotic cells in the dentate gyrus indicative of a change in neuronal survival. These results suggest that the beta 2-subunit containing nicotinic acetylcholine receptors play an important role in regulating cell proliferation in the hippocampus and that endogenous acetylcholine may act to oppose the negative effects of normal aging and stress on cellular proliferation.
%K Aging
%K Animals
%K Apoptosis
%K Cell Division
%K Female
%K Gliosis
%K Hippocampus
%K Male
%K Mice
%K Mice, Inbred C57BL
%K Mice, Knockout
%K Neurons
%K Receptors, Nicotinic
%U http://dx.doi.org/10.1002/syn.20081
%U http://www.ncbi.nlm.nih.gov/pubmed/15472930
%P 200-206

PT Journal
AU Harrist, A
   Beech, RD
   King, SL
   Zanardi, A
   Cleary, MA
   Caldarone, BJ
   Eisch, A
   Zoli, M
   Picciotto, MR
TI Alteration of hippocampal cell proliferation in mice lacking the beta 2 subunit of the neuronal nicotinic acetylcholine receptor.
SO Synapse (New York, N.Y.)
JI Synapse
PD Dec
PY 2004
BP 200
EP 206
VL 54
IS 4
DI 10.1002/syn.20081
LA eng
DE Aging; Animals; Apoptosis; Cell Division; Female; Gliosis; Hippocampus; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Neurons; Receptors, Nicotinic
AB Adult hippocampal neurogenesis declines with age in parallel with decreased performance on a variety of hippocampal-dependent tasks. We measured the rate of cellular proliferation in the hippocampus of mice lacking the beta 2-subunit of the nicotinic acetylcholine receptor (beta 2-/- mice) at three ages: young adult (3 months old), fully adult (7-10 months old), and aged (22-24 months old). Consistent with previous studies, we observed an age-related decline in hippocampal proliferation in both groups. However, in fully adult beta 2-/- mice a 43% reduction of granule cell proliferation was detected compared to age-matched controls. This was accompanied by a significant decrease in dentate gyrus area/section and the length of the granule cell layer in beta 2-/- mice. These alterations were not the result of a change in plasma corticosterone levels or expression of the neurotrophic factor BDNF in the dentate gyrus, two known regulators of hippocampal cell proliferation. Similarly, there was no increase in gliosis, abnormal myelination, or apoptotic cell death in the beta 2-/- animals, although there was a significant shift in the location of apoptotic cells in the dentate gyrus indicative of a change in neuronal survival. These results suggest that the beta 2-subunit containing nicotinic acetylcholine receptors play an important role in regulating cell proliferation in the hippocampus and that endogenous acetylcholine may act to oppose the negative effects of normal aging and stress on cellular proliferation.
ER

PMID- 15472930
OWN - NLM
STAT- MEDLINE
DA  - 20041026
DCOM- 20050103
LR  - 20071114
IS  - 0887-4476 (Print)
IS  - 0887-4476 (Linking)
VI  - 54
IP  - 4
DP  - 2004 Dec 15
TI  - Alteration of hippocampal cell proliferation in mice lacking the beta 2 subunit
      of the neuronal nicotinic acetylcholine receptor.
PG  - 200-6
AB  - Adult hippocampal neurogenesis declines with age in parallel with decreased
      performance on a variety of hippocampal-dependent tasks. We measured the rate of 
      cellular proliferation in the hippocampus of mice lacking the beta 2-subunit of
      the nicotinic acetylcholine receptor (beta 2-/- mice) at three ages: young adult 
      (3 months old), fully adult (7-10 months old), and aged (22-24 months old).
      Consistent with previous studies, we observed an age-related decline in
      hippocampal proliferation in both groups. However, in fully adult beta 2-/- mice 
      a 43% reduction of granule cell proliferation was detected compared to
      age-matched controls. This was accompanied by a significant decrease in dentate
      gyrus area/section and the length of the granule cell layer in beta 2-/- mice.
      These alterations were not the result of a change in plasma corticosterone levels
      or expression of the neurotrophic factor BDNF in the dentate gyrus, two known
      regulators of hippocampal cell proliferation. Similarly, there was no increase in
      gliosis, abnormal myelination, or apoptotic cell death in the beta 2-/- animals, 
      although there was a significant shift in the location of apoptotic cells in the 
      dentate gyrus indicative of a change in neuronal survival. These results suggest 
      that the beta 2-subunit containing nicotinic acetylcholine receptors play an
      important role in regulating cell proliferation in the hippocampus and that
      endogenous acetylcholine may act to oppose the negative effects of normal aging
      and stress on cellular proliferation.
FAU - Harrist, Alexia
AU  - Harrist A
AD  - Department of Psychiatry, Yale University School of Medicine, New Haven,
      Connecticut 06508, USA.
FAU - Beech, Robert D
AU  - Beech RD
FAU - King, Sarah L
AU  - King SL
FAU - Zanardi, Alessio
AU  - Zanardi A
FAU - Cleary, Muriel A
AU  - Cleary MA
FAU - Caldarone, Barbara J
AU  - Caldarone BJ
FAU - Eisch, Amelia
AU  - Eisch A
FAU - Zoli, Michele
AU  - Zoli M
FAU - Picciotto, Marina R
AU  - Picciotto MR
LA  - eng
GR  - AA15632/AA/NIAAA NIH HHS/United States
GR  - DA00167/DA/NIDA NIH HHS/United States
GR  - DA00436/DA/NIDA NIH HHS/United States
GR  - DA10455/DA/NIDA NIH HHS/United States
GR  - DA14241/DA/NIDA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Synapse
JT  - Synapse (New York, N.Y.)
JID - 8806914
RN  - 0 (Receptors, Nicotinic)
RN  - 0 (nicotinic receptor beta2)
SB  - IM
MH  - Aging/pathology/physiology
MH  - Animals
MH  - Apoptosis
MH  - Cell Division/physiology
MH  - Female
MH  - Gliosis/pathology
MH  - Hippocampus/*cytology/*physiology
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Neurons/*cytology/physiology
MH  - Receptors, Nicotinic/*genetics
EDAT- 2004/10/09 09:00
MHDA- 2005/01/04 09:00
CRDT- 2004/10/09 09:00
AID - 10.1002/syn.20081 [doi]
PST - ppublish
SO  - Synapse. 2004 Dec 15;54(4):200-6.
TY  - JOUR
AU  - Harrist, Alexia
AU  - Beech, Robert D.
AU  - King, Sarah L.
AU  - Zanardi, Alessio
AU  - Cleary, Muriel A.
AU  - Caldarone, Barbara J.
AU  - Eisch, Amelia
AU  - Zoli, Michele
AU  - Picciotto, Marina R.
PY  - 2004/Dec/15
TI  - Alteration of hippocampal cell proliferation in mice lacking the beta 2 subunit of the neuronal nicotinic acetylcholine receptor.
T2  - Synapse
JO  - Synapse (New York, N.Y.)
SP  - 200
EP  - 206
VL  - 54
IS  - 4
KW  - Aging
KW  - Animals
KW  - Apoptosis
KW  - Cell Division
KW  - Female
KW  - Gliosis
KW  - Hippocampus
KW  - Male
KW  - Mice
KW  - Mice, Inbred C57BL
KW  - Mice, Knockout
KW  - Neurons
KW  - Receptors, Nicotinic
N2  - Adult hippocampal neurogenesis declines with age in parallel with decreased performance on a variety of hippocampal-dependent tasks. We measured the rate of cellular proliferation in the hippocampus of mice lacking the beta 2-subunit of the nicotinic acetylcholine receptor (beta 2-/- mice) at three ages: young adult (3 months old), fully adult (7-10 months old), and aged (22-24 months old). Consistent with previous studies, we observed an age-related decline in hippocampal proliferation in both groups. However, in fully adult beta 2-/- mice a 43% reduction of granule cell proliferation was detected compared to age-matched controls. This was accompanied by a significant decrease in dentate gyrus area/section and the length of the granule cell layer in beta 2-/- mice. These alterations were not the result of a change in plasma corticosterone levels or expression of the neurotrophic factor BDNF in the dentate gyrus, two known regulators of hippocampal cell proliferation. Similarly, there was no increase in gliosis, abnormal myelination, or apoptotic cell death in the beta 2-/- animals, although there was a significant shift in the location of apoptotic cells in the dentate gyrus indicative of a change in neuronal survival. These results suggest that the beta 2-subunit containing nicotinic acetylcholine receptors play an important role in regulating cell proliferation in the hippocampus and that endogenous acetylcholine may act to oppose the negative effects of normal aging and stress on cellular proliferation.
SN  - 0887-4476
UR  - http://dx.doi.org/10.1002/syn.20081
UR  - http://www.ncbi.nlm.nih.gov/pubmed/15472930
ID  - Harrist2004
ER  - 
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